|Anne Weston/Wellcome Images-- Cancer Cell|
I had seen her a few months before I found my tiny, painful lump signaling my cancer’s recurrence. I remember how upset I was that her trained hands did not find it first. The now five millimeter lump was growing on my chest a few inches below my right clavicle. How did she miss it?
After treatment for this second recurrence ended in December of 2010, life returned to normal, again. I had not seen my surgical oncologist since she surgically removed some extra tissue, to be sure she got it all, after scooping my tiny tumor from my chest right there in her office--as I said, she was swift. Now, since chemotherapy had become a part of my life, someone else was directing my treatment--a general oncologist. My third anniversary from diagnosis was about to be reached. At the time, I was excited about reaching that milestone. For people like me with Her2neu disease, if it is going to recur, I was told, it usually does so in the first 3 years. As time moved along, I was released from seeing my general oncologist every six months to waiting an entire year. Life was good! And, then, there it was. A tiny enlarged lymph node at the front of my neck marking round three of disease and the final chapter of my life telling me I had never been cancer free at all.
When the never-ending treatments for my disease became reality, I couldn’t stop myself from going through the “what if” scenarios. What if the margins between good tissue and cancerous tissue had been bigger after my first surgery? A few millimeters apart just didn’t seem large enough. Since I did not have radiation after my mastectomy because it was only offered to lumpectomy patients, my mind kept circling back to the question: could that have stopped the progression? And, what about those dormant cells that no one has control over. Maybe those cells never awakened therefore making the infusions useless. Maybe if I had been treated for a longer time period that would have made the difference.
There are simply too many variables and no way to ever know if anything could have been done differently to stop me from becoming stage four. It is all a guessing game based on statistics gathered through clinical trials. Contemplating all the “what if’s” and my participation in the “blame game” felt justified. I thought I had been wronged. Ductal Carcinoma In-Situ wasn’t supposed to become metastatic yet that is exactly what had happened. My mental battlefield kept telling me, well if only this had happened, I would be okay. It was absolutely pointless.
Today, the more I research and read, the more I learn. Because of that, any anger I held toward my surgeon or any of my doctors has softened over time. In those readings I have found a few studies giving researchers reason to suspect that some breast cancers, especially the her2neu type like mine, are metastatic long before a lump or other physical abnormality of the breast can be found either by the patient or a detection device. Metastasis may even begin at the initial onset of disease.
Here is a recent article about early metastasis: here by Sharon Begley @sxbegle, December 14, 2016, entitled Cancer cells spread way earlier than thought, seeding metastases that cause most deaths.
This is an excerpt:
“Earlier research had hinted that some cancer cells set out for distant organs long before a tumor is detectable. A 2008 mouse study, here led by Christoph Klein of Germany’s University of Regensburg, who also led one of the new studies here found that cancer cells reached the bone marrow months before breast tumors formed. A 2011 study of 30 women with “non-invasive” breast cancer found that eight actually had cancer cells in the bone marrow. In about 8 percent of non-invasive breast cancers, a 2015 study here reported, metastases develop — even though “non-invasive” means the malignant cells can’t enter the bloodstream and travel to vital organs." . .
. . . "The new studies were done in lab mice. The study at Regensburg found that in mice given the human breast cancer gene HER2, the hormone progesterone triggers the migration of cancer cells almost as soon as they form — that is, before a tumor is detectable. And these early émigrés are better at forming metastases than cancer cells that depart the tumor later.
At Mount Sinai, Aguirre-Ghiso found that a gene called p38 acts as a brake on the departure of cancer cells from still-forming breast tumors. When p38 is silenced and HER2 is activated, the combination awakens molecules that, eventually, mobilize cancer cells into the bloodstream and on to the lungs and bones.”
Frightening, isn't it?
With this new information any anger still quietly lingering within me vanished. If this proves to be true, all of the therapies I have undergone from the beginning never could have been enough to stop the one mutated cell (or cells) floating in my lymphatic system or blood stream while waiting to lay claim on a distant organ. It wasn't enough to stop those cells that had left my breast years before there was any indication of disease. Catching my disease at stage 0 seems early, doesn't it? But, for some of us, early may not be early enough.
For further reading see links below: